APPENDIX
I-S: Crinnion, Environmental Medicine, Part 4:
Pesticides – Biologically Persistent and
Ubiquitous Toxins, Page 432 Alternative Medicine Review _ Volume 5 Number 5 _ 2000
This appendix is copied from:
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Environmental Medicine, Part 4:
Pesticides – Biologically Persistent and
Ubiquitous Toxins.
Walter J. Crinnion, ND
Abstract
Although
the use of pesticides has doubled every ten years since 1945, pest damage
to
crops is more prevalent now than it was then. Many pests are now pesticide
resistant
due to
the ubiquitous presence of pesticides in our environment. Chlorinated pesticide
residues
are present in the air, soil, and water, with a concomitant presence in humans.
Organophosphate
and carbamate pesticides—the compounds comprising the bulk of
current
pesticide use—are carried around the globe on air currents. Municipalities,
schools,
churches, business offices, apartment buildings, grocery stores, and
homeowners
use pesticides on a regular basis. Pesticides are neurotoxins that can
cause
acute symptoms as well as chronic effects from repeated low-dose exposure.
These
compounds can also adversely affect the immune system, causing cell-mediated
immune
deficiency, allergy, and autoimmune states. Certain cancers are also associated
with
pesticide exposure. Multiple endocrine effects, which can alter reproduction
and
stress-handling
capacity, can also be found. Limited testing is available to assess the
toxic
overload of these compounds, including serum pesticide levels and immune system
parameters.
Treatment for acute or chronic effects of these toxins includes avoidance,
supplementation,
and possibly cleansing.
( Altern Med Rev 2000;5(5)432-447)
Introduction
The objective of pesticide use to prevent crop loss from
insects remains unachieved. K.
Ausubel in his book, Seeds of Change, The Living
Treasure, notes that since 1945 overall pesticide
use has risen 3,300 percent, while overall crop loss due to
insects has risen 20 percent in the
same time period.1 Ausubel reminds us about Martin
Borlaug and the “Green Revolution,”
which introduced F1 hybrid seeds that provided exceptional
crop yield when augmented by
utilizing high nitrogen fertilizer. To protect plant
growth, herbicides were needed to prevent
weeds from competing for nutrients and space, as well as
pesticides to prevent pest-induced
crop damage.
The killing of primary pests with pesticides has paved the
way for secondary pests to
come to the fore. Where previously there were 10 primary
pest insects – defined as causing
greater than one million dollars of crop damage per year –
there are now 300. Of the 25 most
serious pests, 24 were previously secondary pests and 72
percent of these are now pesticide
resistant.1
Walter Crinnion, ND – Healing Naturally, 11811
NE 128th St, Ste 202, Kirkland, WA 98034.
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Pesticides
Alternative Medicine Review _ Volume 5, Number 5 _ 2000 Page 433
Non-Occupational Pesticide
Exposure
Of the 2.5 million tons of pesticides
used worldwide each year, less than 0.1 percent
reaches the target pest.2,3 Thus, 99+ percent
of currently applied pesticides are being
released indiscriminately into the environment,
many of which will persist for years and travel
far from the point of application.
Chlorinated pesticides found in the soil
can persist for decades. Dichlorodiphenyltrichloroethane
(DDT- see Figure 1) has
been shown to accumulate in soils where it
was used agriculturally.4 Soil-based DDT is
incorporated into grasses growing in the soil,
into cattle consuming the grass, and eventually
into the milk and fat tissue of the cows.5
While the half-life of DDT had been thought
to range between 4-30 years, evidence from
the Yakima River drainage in Washington
State, and in other areas, points to a much more
extended half-life.6 The studies in this area
show increased levels of p,p’-DDT in the soil
and the persistence of ratios of p,p’-DDT: o,p’-
DDT found in the parent compound applied
25 or more years earlier. This indicates that in
certain soils DDT degradation is not occurring
as rapidly as previously thought.
Such persistence has been found in
other areas of the United States, such as soil
in Texas and New Mexico.7 When soil previously
used agriculturally is excavated to accommodate
housing sites, DDT finds its way
into nearby streams and rivers via erosive runoff.
The study of the Yakima River drainage
found DDT in 100 percent of the fish sampled
from that river. Other rivers, such as the South
Platte, show a multitude of organochlorine
pesticides in both sediment and fish.8
When houses are built on previously
contaminated land, pesticides can easily be
brought from the soil (from residents merely
being “outside,” from working in the garden,
etc.) into the house, where they contaminate
the home as house dust, as previously shown
to do.9 Pesticide exposure via house dust has
been shown to cause higher serum levels of
pesticides than what is incurred by eating contaminated
foods.10 There is also the possibility
of pesticide contamination of vegetables
grown in the home garden.
Those compounds not trapped in soil,
tree bark, sediment, animals, humans, or other
stable material begin a wind-driven leapfrogging
around the globe.11 Volatile chemicals
move more frequently whenever the ambient
temperature is sufficient to volatilize them.
Less volatile compounds, like DDT, stay in
place longer before being volatilized again.
Residues of DDT and other halogenated
compounds have been found in medicinal
herbs picked in the forests of Poland and
Germany, where no spraying of DDT in these
areas has been reported.12,13 In a Polish study,
herbs from all regions of the country were
found to contain pesticide residues. The authors
concluded, “Pesticide contents in most
of the herbal raw materials should be attributed
to the global contamination of the environment.”
When these compounds reach upper
latitudes and colder temperatures, they precipitate
from the air and tend to stay trapped in
whatever material they settle in. This has led
to high amounts being found in the mountains
of
recently even Aleutian eagles’ eggs.16 It
likely
accounts for the high amounts of toxins found
in breast milk of indigenous Inuit mothers subsisting
on traditional diets.17 Decades of precipitation
of airborne chlorinated pesticides in
the
of these residues throughout the food chain,
ultimately being transferred to Inuit infants
through breast milk.
Fortunately, 120 countries currently
participating in the United Nations Environmental
Programme are negotiating agreements
for global action on the movement of pesticides
and other chemical pollutants from one
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country to another.18 It is hoped such agreements
will lead to lower levels of airborne traveling
toxins. Unfortunately, this effort does not
address current pesticide loads found in every
part of the planet.
Pesticides of every category have been
found in groundwater throughout the United
States. The U.S. Geological Survey’s analysis
of groundwater found pesticides in the water
from agricultural areas,19 and large amounts
of pesticides have also been found in urban
waterways, primarily due to frequent overapplication
by homeowners. The Mercer
types of pesticides.20 Pesticide residues
are also found in foods; the 12 most contaminated
fruits and vegetables being strawberries,
bell peppers, spinach, cherries (
cantaloupe (Mexican), celery, apples, apricots,
green beans, grapes (Chilean), and cucumbers.
The choice exists, of course, to either
find alternative, less-contaminated fruits and
vegetables, or purchase organic varieties of
these items; however, given existing global
pollution levels, food labeled “organically
raised” does not necessarily mean “pesticidefree.”
Foods grown without pesticides can absorb
pesticides from the soil, or be exposed to
them in the air while growing, or during packing
and transportation. Some foods, such as
squash and carrots, may actually concentrate
chlorinated compounds from the soil while
growing.
While adults can make an informed
choice about what foods to eat, infants cannot.
While there are numerous beneficial aspects
of breastfeeding, numerous studies have
shown persistent chlorinated pesticide residues
in breast milk. This startling fact has been recorded
in tests of breast milk around the globe,
including
28
Kong,32
37
New York42
in the
(including DDT, DDE
[Dichlorodiphenyldichloroethylene] and DDD
[dichlorodiphenyldichloroethane]) have been
found in 93-100 percent of the milk samples
in these studies.
High levels of polychlorinated biphenyls
(PCB) and hexachlorocyclohexanes
(HCH) – also referred to as BHC – are also
frequently found. The majority of these studies
also found numerous other chlorinated
compounds, including hexachlorobenzene
(HCB), endrin, dieldrin, and various
chlordanes.
Most contaminated breast milk
samples have a combination of many such
compounds. All studies had samples that exceeded
the World Health Organization’s acceptable
daily intake of 0.005 mg/kg/day. Levels
of these compounds in breast milk were
shown to correlate directly with the level of
such compounds in maternal adipose tissue.
Furthermore, infant serum levels of pesticides
were shown to correlate with maternal breast
milk levels, and not with airborne exposure.
Pesticide levels in the milk and adipose tissue
of mothers decreased with each breast-fed
child.
Maternal pesticide exposures from diet
or airborne sources have been associated with
maternal load. However, a study in Papua, New
Guinea, was conducted in an area where there
had been no DDT use, yet all lactating women
had DDT in their breast milk. This was most
likely due to the previously discussed movement
of DDT on global air currents. Since
pesticides can bioaccumulate over decades,
and can be passed to the next generation
through both cord blood and breast milk,23 the
implication is that each succeeding generation
begins life with a pesticide load it took their
parents decades to develop.
Children can also be exposed to organophosphate
pesticides (OP), such as
chlorpyrifos, from home use of this compound.
It was demonstrated that after a single broadPesticides
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cast in apartment rooms of this pesticide by
certified applicators (not the typical homeowner),
chlorpyrifos continued to accumulate
on children’s toys and hard surfaces for two
weeks after spraying.43 Based on this and similar
studies it was estimated that after indoor
spraying, children were exposed to levels from
21-119 times the current reference dose of 3
µg/kg/day.44
From these and others studies that
found birth defects associated with
chlorpyrifos,45 the U.S. Environmental
Protection
Agency recently banned home use of this
compound and imposed tighter restrictions on
the pesticide’s use on some agricultural products,
specifically apples and grapes, and
banned its use on tomatoes. These restrictions
are designed to eliminate the chemical’s residues
on foods often consumed by children. The
pesticide may still be used on a variety of
grains and other crops; however, retail sale will
be stopped after December 31, 2001. Despite
overwhelming scientific evidence, no recall of
existing stock was issued.
Pesticide Presence in Human
Adipose Samples
Studies examining general populations
for chlorinated pesticide residues have found
the presence of multiple chlorinated hydrocarbons
(DDT, DDE, DDD, aldrin, dieldrin, heptachlor,
heptachlor epoxide, and PCBs) in the
adipose tissue of residents of Greenland and
Denmark.46
Adipose samples from women in
Germany, The Netherlands, Northern Ireland,
Spain, and Switzerland, as part of the European
Study on Antioxidants, Myocardial Infarction
and Cancer of the Breast, showed the
consistent presence of DDE.47
An adipose study of 40 autopsied
trauma victims in Israel revealed DDE in all
40, HCB in 34, beta hexachlorocyclohexane
in 27, DDT in seven, and gamma HCH in two.
Three or more chlorinated residues were found
in 80 percent of all studied.48
Samples of adipose tissue and other
fluids taken from 17 caesarean section deliveries
in Germany and Tanzania revealed chlorinated
residues in all women. Those from
Germany had higher levels of HCB and PCBs,
while those from Tanzania had higher levels
of DDT and DDE.49 This study found maternal
adipose tissue contained a 10 to 100-fold
increase in accumulation of chlorinated hydrocarbons
compared to other tissues and fluids
tested. The concentration of certain toxins was
higher in fetal cord blood and the placenta than
in the maternal serum. These persistent chlorinated
pesticide residues have also been found
in adipose tissue throughout North and South
America.50-54
The above-mentioned studies all investigated
biologically persistent chlorinated hydrocarbons.
Such tests for determining the
presence of the non-biologically-persistent
organophosphate, carbamate, and pyrethroid
pesticides are not available, although the metabolite
of chlorpyrifos, one of the most common
organophosphates, was found in the urine
of 82 percent of U.S. adults.55 However, these
studies provide a clear indication that more
than the toxic effect of a single pesticide must
be considered. Based on the above-mentioned
studies, the average person, wherever they live
in the world, most likely has more than one
chlorinated hydrocarbon residue in their adipose
and serum components. To this load can
be added any of the organophosphate, carbamate,
pyrethroids, or arsenical pesticides that
may be in the air, food, or water, as well as
solvents, heavy metals, polycyclic aromatic
hydrocarbons (from combustion of fossil fuels,
wood, cigarettes), terpenes, molds, etc.
Neurotoxicity of Pesticides
Pesticides kill insects by disrupting the
nervous system. The primary action of chlorinated
pesticides – which includes endrin, aldrin,
toxaphene, benzenehexachloride (BHC),
HCH, DDT, heptachlor, heptachlor epoxide,
chlordane, trans-nonachlor, polychlorinates,
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dicofol, chlorobenzilate, mirex, HCB, methoxychlor
and ethylan – is interfering with axonal
transmission by disrupting ion flux, leading
to over-stimulation of the nerves and uncontrolled
neuronal discharge. Symptoms of
acute human toxicity include headache, nausea,
vomiting, hyperesthesias, irritability, confusion,
convulsions, respiratory depression,
cardiac arrhythmia, aplastic anemia, and porphyria
cutanea tarda.
DDT, the best known of this class, was
synthesized in 1874. Its pesticide activity was
found in 1939, and it was used extensively by
the U.S. military in World War II to control
typhus, malaria, and lice. It was put into use
in U.S. agriculture in 1945, and subsequently
banned in 1974 after the uproar caused by
Rachel Carson’s publication of Silent Spring.
In certain individuals DDT has been shown to
cause changes in electromyographic potential
and symptoms of fatigue, poor cognition, withdrawal
from reality, blurred vision, headache,
and ataxia.56,57
Levels of gamma HCH and dieldrin
have been found to be higher in the brain tissue
of persons with Parkinson’s disease than
in controls.58
Elevated levels of DDE were also
found in the substantia nigra in these
Parkinson’s patients. Lindane (gamma HCH)
blocks the chloride ion channel by antagonizing
GABA stimulation of chloride ion uptake
through benzodiazepine receptors.
Lindane can dramatically reduce the
time needed for establishing CNS kindling,
lower the convulsive threshold,
and prolong the sensitivity to convulsive
stimuli even after its clearance
from the blood.59 Having such potential
for increasing seizure activity, it
is surprising Lindane is allowed in
shampoo treatments for head lice in
children and adults.
The OP pesticides were first
synthesized in 1820. These compounds
were developed by Germany
as nerve gases for military use during
World War II. Their present-day nerve gas relatives
include Sarin, recently used in a Japanese
terrorist attack in the Tokyo subway system.
60 They
were first used as pesticides in
1941-1944.
OP pesticides are rapidly absorbed following
inhalation or ingestion. Dermal absorption
is slower but prolonged exposure can result
in severe poisoning. Once absorbed, OP
compounds accumulate in fat, liver, kidneys,
and salivary glands.61 Instead of affecting axonal
transmission, as chlorinated hydrocarbons
do, they are acetylcholinesterase (AChE) inhibitors
via phosphorylation. This leads to accumulation
of acetylcholine, which binds to
and stimulates muscarinic receptors (found in
autonomic ganglia, CNS, heart, salivary
glands, and smooth muscles) and nicotinic receptors
(autonomic ganglia, skeletal muscle,
and CNS). The brain initially over-stimulates;
later there is paralysis of neural transmission.
Antibodies to the cytochrome P450 hepatic
detoxification system are also generated.
OP toxicity is heightened by the presence
of the solvents toluene and xylene, which
are found in some commercial OP products as
“inert ingredients.” Synergistic toxicity is also
found with OP compounds and polycyclic aromatic
hydrocarbons from auto exhaust.62 The
combination of neurotoxicity of solvents and
Figure 1: Dichlorophenyltrichloroethane (DDT)
CCl3
Cl Cl
Pesticides
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organophosphates can cause axonal and myelin
degeneration in distal fibers. Their neurotoxic
effect may be more pronounced in older
individuals, partly due to the normal decline
of AChE with aging.63 Neonatal exposure to
both OP and chlorinated pesticides appears to
potentiate the neurotoxic effects if re-exposure
occurs later in life.64
Symptoms of acute organophosphate
poisoning include (1) nausea, vomiting, abdominal
cramps, and diarrhea; (2) salivation
and rhinorrhea; (3) headache and vertigo; (4)
fixed pinpoint pupils, blurred vision, and ocular
pain; (5) muscle twitches (face, tongue, and
neck); (6) difficulty breathing (from excess
secretions); and (7) respiratory paralysis and
death.
The acronym “SLUDGE” – for salivation,
lacrimation, urination, defecation, gastrointestinal
disturbances, and emesis – is often
used for the toxic picture of these compounds.
If the antidote pralidoxime (2-PAM)
is not given within 24-48 hours, the AChEphosphate
bond becomes so strong that physiologic
recovery depends on new synthesis of
AChE. AChE is restored to the affected area
in about two weeks, but in the whole body it
can take up to three months to recover. Serum
testing for red blood cell AChE levels is often
inconclusive except in the most serious poisonings.
One study looked at both central nervous
system effects via SPECT scans and red
blood cell cholinesterase levels. Patients were
differentiated into three groups, latent poisoning,
mild and moderate poisoning, and severe
poisoning. While all groups showed CNS damage
on SPECT scans only the severe poisoning
group had AChE levels below normal.65
Ishikawa has studied organophosphate
poisoning in Japan, and found that in addition
to being neurotoxic, OPs cause severe oxidative
damage and stress, resulting in decreased
selenium concentration in the brain and kidneys
within 14-21 days of exposure.66 He also
found docosahexanoic acid (DHA) (animals
15 mg/kg/day, humans 5mg/kg/day), but not
eicosapentaenoic acid (EPA), crossed the
blood-brain barrier and prevented a rise in superoxide
radicals secondary to OP exposure.
The areas of greatest oxidative damage were
the eyes (including optic nerve atrophy,
neuroretina, and the destruction of retinal pigment),
brain, and heart. Neurological changes
unrelated to AChE inhibition include behavioral
abnormalities, anxiety, irritability, confusion,
depression, and fatigue.
Carbamates are also AChE-inhibiting
pesticides, but they accomplish this by reversible
carbamylation, not phosphorylation.
SLUDGE symptoms can still be present, as
carbamates primarily affect muscarinic and
nicotinic receptors.
Chronic CNS symptoms have been frequently
reported after repeated exposure to OP
and carbamate compounds. Exposed greenhouse
workers exhibited longer reaction times
and reduced motor steadiness as well as increased
tension, depression, and fatigue.67
When matched with controls, workers in a factory
making OP pesticides showed no difference
in AChE levels but did show greater problems
with memory, learning, and vigilance.68
Sheep ranchers exposed to OP compounds in
the course of sheep dipping exhibited poorer
sustained attention and speed of information
processing than non-exposed controls. The
ranchers also showed greater vulnerability to
psychiatric disorders than controls.69
When compared with controls, workers
applying termiticide demonstrated poorer
performance on pegboard turning tests and
postural sway tests. They also displayed significantly
more symptoms of memory disturbances,
altered emotional states, fatigue, and
loss of muscle strength.70 Such neurotoxic effects
can be found years after a single OP poisoning
episode. Thirty-six such individuals
were re-evaluated two years after a single episode
of unintentional OP intoxication. On reexamination
the poisoned group did worse
than the control group on all neuropsychological
subtests, as well as other tests for verbal
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and visual attention, visual memory,
visuomotor speed, sequencing, problem solving,
motor steadiness, and dexterity.71
Animal studies have shown that inutero
exposure to OP compounds result in
impairment on maze performance, locomotion,
and balance in neonates.72
Peripheral neuropathy is also a common
sequelae of OP exposure. South African
farm workers exposed to OP pesticides who
reported significantly more problems with dizziness,
sleepiness, and headache were also
found to have reduced vibratory sense and increase
in hand tremor.73 Flower bulb farmers
were noted to have decreased conduction velocity
of fast and slow motor fibers of the median
and peroneal nerves as well as sensory
fibers of the median and sural nerves.74
Ecuadorian pesticide applicators exhibited
a significantly greater incidence of poor
coordination, abnormal deep tendon reflexes,
and reduced strength than non-exposed local
controls.75
Of 217 chlorpyrifos poisoning incidents
reported by DowElanco, 21 cases had
some evidence of peripheral neuropathy.
Symptoms of delayed neuropathy typically
show up several days to four weeks after
acute organophosphate exposure. Early signs
are paresthesias, weakness and ataxia, gait
changes, or flaccid paralysis. Some of the
chronic neurotoxic effects of OP pesticides
may be due to their ability to induce the formation
of antibodies to neuronal tissues. Antibodies
to myelin basic protein, neurofilament
triplet protein, and glial fibrillary acidic proteins
have all been exhibited after OP exposure.
76 Other
antibodies to smooth muscle,
parietal cells, brush borders, and thyroid have
been demonstrated, as well as antinuclear antibodies.
77
Immunotoxicity of Pesticides
The patient with chronic environmental
pesticide overload generally presents to the
clinician with either the above-mentioned neurotoxic
manifestations or those of
immunotoxicity. Different pesticides can cause
varying effects on the immune system of any
given individual. However, in viewing the
overall effect, toxin exposure causes a specific
immunologic imbalance unseen by other causative
agents, including a general decrease in
cell-mediated immunity (CMI) and an increase
in humoral immune response.79-82 The reduction
in CMI can include reductions or elevations
of T cell counts, including natural killer
cells, depending on the specific compound.83
In general, chemotactic and phagocytic responses
are significantly reduced. Many chlorinated
compounds also cause reduction of
thymic weight and function. Natural killer cell
activity is universally reduced.
These changes result in the clinical
picture of decreased resistance, and an increase
in allergies and certain cancers. The elevation
of humoral immunity often results in production
of antibodies to various tissues, as previously
mentioned,77
and is also seen in exposure
to chlorinated pesticides.84 The
immunotoxic effects can be modulated by several
factors, including level of exposure, nutritional
status (low protein), concurrent pathologic
conditions, biotransformation and activity
of metabolites, physical and emotional
stress, and oxidative stress.85 Both OP and chlorinated
pesticide exposure have been associated
with chronic fatigue syndrome.86,87
One of the most published and contested
arenas of pesticide-induced
immunotoxicity is the area of oncology. Some
studies looking only at DDT exposure and serum
levels have failed to show any significant
increase in cancer mortality or long-term
health effects.88,89 However, when the large
picture of pesticide use is viewed, a positive
correlation with cancers is noted.90 Pesticide
exposure causes DNA damage and the formation
of DNA adducts, which can ultimately
lead to cancer formation.91
OP pesticide use has been associated
with aplastic anemia and leukemia in exposed
farmers,92,93
and in children exposed from
Pesticides
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having their homes treated.94 The studies
involving
children revealed a positive association with
both OP and pyrethroid pesticide exposures
and these hematologic disorders. Increased
rates of multiple myeloma have also been
associated with OP exposure.95 Chlorinated
pesticides are positively associated with the
incidence of non-Hodgkin’s lymphoma,96-98
aplastic anemia,99 cancers of the liver, colon/
rectum, and lung,100,101 multiple myeloma,102
pancreatic cancers,103,104 blood dyscrasias and
leukemia,105
and acute myeloid leukemia
(along with solvent exposure).106,107
The issue of the association of chlorinated
products with breast cancer has been the
subject of numerous studies, and is beyond the
scope of this article. Many studies have found
a positive association between breast cancer
and chlorinated pesticides108-116 and many have
not.117-120
In the positive studies, associations
have been made between breast cancer and
adipose levels of DDT, DDE, PCB, dieldrin,
and HCH.
While this question seems far from
being settled it appears obvious that pesticide
load in some women may be a factor in the
development of breast cancer. A recent study
showed that women with a genetic polymorphic
variant of cytochrome P450-1B1 – which
catalyzes the formation of 4-hydroxyestradiol
that retains significant estrogenic activity and
whose metabolites can generate potentially
mutagenic free radicals that may damage DNA
– have a greatly elevated risk of breast cancer.
121 It was
noted that polycyclic aromatic
hydrocarbons and chlorinated pesticides are
all known inducers of CP450. Such an induction,
associated with genetic polymorphism,
might partly explain why pesticides are an
apparent risk factor in some women but not
others.
Endocrine Toxicity from Pesticides
After symptoms appear in the immunological
and neurological realms, problems
in endocrine function may also occur. Such
hormonal imbalances are rarely the first to be
noted when taking a chronological medical
history. Chlorinated products are known to act
as weak estrogens with potential for reproductive
disruption122
and to act as androgen antagonists.
123 These
compounds have been associated
with female infertility,124 miscarriages,
125 and
possibly male infertility.126 OP
pesticides have also been associated with male
infertility, with increased LH production (possibly
secondary to testicular damage),127 and
reduced numbers of morphologically normal
and live spermatozoa.128
In addition to possibly affecting reproduction,
pesticides can cause other endocrine
problems. HCH, but not DDT, has been shown
to modify pineal synthesis of melatonin.129
DDE, the metabolite of DDT, can accumulate
in the zona fasciculata in the adrenals130 and
lead to adrenal atrophy.131 In animal models
vacuolization and necrosis in the zona
fasciculata secondary to DDE exposure appears
most profound in fetal and neonatal animals,
and less so in adults. The DDT metabolite
also appears to be a tissue-specific toxicant
to the zona fasciculata.132 Reviews on
these and other endocrine effects from environmental
chemicals can be found in the literature.
133,134
Other published health effects from
pesticides include renal tubular toxicity from
an OP compound accompanied with elevated
hydrogen peroxide production and increased
lipid peroxidation.135 This again shows the
extensive oxidative damage that OP compounds
can cause. OP compounds have also
been linked to reduced bone formation.136 Agricultural
workers exposed to OP compounds
had significantly decreased bone formation
than healthy controls.
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Clinical Assessment
It should be recognized that all individuals
are exposed to pesticides and that all
carry some level of these toxins in their serum
and adipose tissue. In addition, numerous
variations in genetics, diet, lifestyle, and environment
can interplay to either facilitate or
conspire against clearance of these compounds
from the body. Once a chronological medical
history is obtained, the classic pattern of neurotoxicity
and immunotoxicity, possibly followed
by endocrine toxicity, may be seen.
Once seen or suspected, testing may be warranted.
Because chlorinated compounds are fat
soluble and bioaccumulative they can be easily
measured in serum. This can be done either
fasting or non-fasting, although non-fasting
samples tend to show higher levels.137 Most
authors recommend the lipid content of the
blood be looked at simultaneously so compounds
can be rated as per gram of lipid. This
provides the best correlation with adipose
samples. However, serum and adipose
samples can be vastly divergent.
Table 1 shows the variance between
serum and adipose samples from one individual.
If an adipose sample is to be taken,
it is recommended that adipose tissue be
taken from three different sites, as toxin distribution
is uniform. Laboratories that specialize
in testing these compounds do not
give results in amount of toxin per gram of
lipid as the literature suggests, but in ng/ml
of blood. The laboratories also provide levels
of their laboratory averages as a reference
range. These are the averages of tests
done by the specific laboratory, and do not
necessarily represent “normal ranges” in the
These laboratories also perform
urine analysis for metabolites of organophosphates
and carbamates. These compounds
are generally cleared from the urinary
tract within 14 days of exposure and
do not show exposure prior to that time. As
mentioned earlier, testing for red blood cell
acetylcholinesterase levels is generally not
definitive except in cases of serious poisoning.
Some laboratories also offer testing for
autoantibodies that can be formed from exposure
to pesticides and solvents. Testing of immune
parameters, including lymphocyte subpopulations
and natural killer cell activity, may
also give an indication of immunotoxicity.
Treatment for Chronic Pesticide
Exposure
The first step in treating any toxic individual
is avoidance of further exposure. Recognizing
that pesticide use is ubiquitous, this
may not be easy. Avoidance can include consuming
organic foods, avoiding living in or
traveling through agricultural areas during
spraying seasons, avoidance of public buildings
after spraying has taken place, finding out
Table 1: Chlorinated Pesticides in Serum
and Adipose Samples (parts per billion).
Courtesy of Accu Chem Laboratories.
Compound
Serum Adipose
HCB
<0.3 135
Endrin
<0.3 168
Beta-BHC
<0.3 1657
Gamma-BHC
<0.3 121
Heptachlor
<0.3 63
Hep-Epoxide
<0.3 33
Oxychlordane
0.4 72
Trans-nonachlor
0.3 123
Dieldrin
<0.3 36
DDE
14.2 284
DDT
<0.3 222
Pesticides
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when neighbors or governmental agencies are
planning to spray an area, etc.
In addition, it should be determined
whether their present dwelling had been termite-
treated (chlordane has a half-life of 20
years) or had other pesticide treatments. Carpeting
from previous owners when the dwelling
was treated would contain pesticide residues,
as would the dust in furnace ducts, both
of which would need to be remediated. The
fewer pesticides personally used, and the fewer
foods or other consumer products purchased
that rely on pesticide use will ultimately reduce
the amount of pesticides released into the
atmosphere.
The second treatment step is supplementation
of the nutrients needed to help clear
pesticides from the body, restore common pesticide-
induced deficiencies, and prevent tissue
damage from these compounds. Dietarily,
adequate protein and reduced sugar intake
ensures proper liver clearance of xenobiotics
from the blood. Whey protein increases glutathione
levels in addition to providing complete
protein to the body, which enhances
liver function, making it the first choice for
such cases. Chlorinated pesticides and other
chlorinated compounds reduce the available
vitamin A and thiamine to normal tissues,
the deficiency of which tends to increase the
toxic effect of pesticides.
In addition to these nutrients, a high
quality multiple vitamin/mineral supplement
with extra magnesium, pyridoxine, selenium,
antioxidants, and milk thistle is recommended.
Vitamin C should be taken in
maximal doses to help clear toxins from the
blood and to provide high antioxidant activity.
Docosahexanoic acid (DHA) is necessary
for any OP exposure to increase antioxidant
activity in the brain and prevent OPinduced
damage.
If elevated levels of chlorinated pesticides
are found in serum or tissue, additional
measures may be necessary, such as
the frequent use of low temperature saunas,
hydrotherapy, and colonic irrigation.138
Summary
Pesticides are ubiquitous in the environment.
Residues of chlorinated pesticides
are present in the air, soil, and water, as well
as in most humans. Organophosphate and carbamate
pesticides—the compounds comprising
the bulk of current pesticide use—are carried
around the globe on air currents. These
pesticides are used in schools, churches, business
offices, apartment buildings, grocery
stores, and homes on a regular basis. Pesticides
are primarily neurotoxins, causing both
acute symptoms as well as chronic effects from
repeated low-dose exposures. These compounds
adversely affect the immune system,
primarily causing cell-mediated immune deficiency,
allergy, and autoimmunity. Multiple
Pesticide Protection and Detoxification.
• Avoid Further Exposure
• Nutritional Supplementation
Adequate
protein (whey preferably)
Decrease
sugar intake
Vitamin
A
Vitamin
B1 (Thiamine)
Magnesium
Vitamin
B6 (Pyridoxal 5’-phosphate)
Selenium
Antioxidants
Silybum
marianum (milk thistle)
Vitamin
C
DHA
• Adjunctive Therapies
Low-temperature
sauna
Hydrotherapy
Colonic
irrigation
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endocrine effects can alter reproduction and
stress-handling capacity. Laboratory testing to
determine if a toxic pesticide overload exists
is limited to serum pesticide levels and immune
system parameters. Treatment for pesticide
toxicity includes avoidance, nutritional/botanical
supplementation, and detoxification/
cleansing.
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